Peptic Ulcer Disease

Approximately 10% of the US population experience peptic ulcer disease, which has significantly impacted the health care system; both men and women appear to be affected equally with the condition. Peptic ulcer disease may lead to several complications, including an upper gastrointestinal hemorrhage.

00:01
Our topic now brings us into Peptic Ulcer Disease.
With peptic ulcer disease, you divide this intothat disease or erosion that's taking place in the
stomach versus that type of erosion that might betaking place in duodenum. By far in the US, the most
common type of peptic ulcer disease would be thetype that’s taking place in the duodenum. However,
for learning purposes, we need to make sure that wecover both sets of peptic ulcer disease. And then
importantly, we will go through the symptoms of yourpatient so that you’re able to distinguish one from
the other. Mechanism of injury. If there’s directmucosal damage due to toxins, ethanol, NSAIDs,
bile or H. pylori. Now for the most part,you can think of peptic ulcer disease taking place
in the stomach as really not due to increasedacid production. Remember that the stomach is extremely
effective with protecting the lining of the stomachfrom the acid. And due to all that bicarbonate, your
prostaglandins and such so therefore protecting thestomach from all that acid. However, if the lining
of the stomach has been compromised where it couldtake place due to let’s says, NSAIDs which is then
inhibiting your COX pathway. Then you might theninhibit the formation of the prostaglandin necessary
to properly protect or contribute to the protectionof the stomach. Or, if there is actual chemical
damage taking place to the lining of the stomachdue to bile that might then regurgitate back into
the stomach. Remember bile is being released orsecreted from your gallbladder into the second part
of the duodenum. So therefore, there must be somekind of method by which the bile is retrograde flow
back in the stomach causing damage. H. pylori in thestomach would be residing where?In the antrum of the stomach. And from henceforth
whenever we deal with H. pylori, you should be thinkingeither the distal end of the stomach or the first part
of the duodenum as being its place of residence.
02:15
In the stomach, the H. pylori if you remember
from micro, then has an enzyme called urease.
02:20
Therefore it will take the urea and they will create
a force field for itself. That force field that theH. pylori then creates in the antrum of the stomach
is then made up of ammonia. Amazing, isn’t it?At some point in time, it could then burrow into the
lining of the stomach and so therefore weakening thelining resulting in peptic ulcer disease. H. pylori,
bile, NSAIDs, alcohol. Prostaglandin inhibition likewe just said with NSAIDs or steroids even with
pathologies such as Cushing in which you would haveexcess cortisol. Hypercortisolism, is then knocking
out your phospholipase A2. You don’t have thenecessary prostaglandin to protect the lining of
the stomach and such against the acid.
03:07
Increased acid production could be a cause. But more
importantly, the most important pathogenesisfor peptic ulcer disease of the stomach would be
damage to the lining. Whereas if it is pathogenesisfor peptic ulcer disease of the duodenum, then in
fact there would be increased acid. For example,if you do Zollinger-Ellison syndrome and with the
gastrinoma, with all that acid which is thencoming out like a huge wave out of the stomach and
into the duodenum. There is no way that the duodenumcan properly protect itself against all that acid.
Mucosal ischemia is always a possibility wheneverthere is infarction that’s taking place. And then at some
point in time you might then be hurting or injuringthe lining of the stomach. Peptic ulcer disease, if
it is in the stomach, the patient here is going tobe complaining of epigastric pain. However this time
around, with peptic ulcer disease in the stomachyou would not find and the patient would not be
complaining of pain that’s radiating to the back.
04:12
Is that clear? On your step and on your wards, if
the pain is radiating to the back then this gives youthe high suspicion and differential of pancreatic
damage. However if it’s not then you’re thinking aboutpeptic ulcer disease. Also with this erosion that’s
taking place, remember, you have not perforated.
04:33
Ulceration means ulceration. It’s a clean, punched
out lesion in the stomach. And a clean, punched outlesion, here, with bleeding taking place may result
in hematemesis. With all this blood that’s nowbeing released either from the stomach or maybe
perhaps the duodenum, you can only imagine thatas I told you earlier that the stool has an
opportunity to completely saturate itself with blood.
05:02
So therefore by the time it’s evacuated, here the
stool in fact is going to look black and tarry.
05:09
Hematemesis, hematochezia, iron deficiency anemia,
all these, well, all part of bleeding.
05:17
Next, if there is perforation that’s taking place
especially of the duodenal type of peptic ulcer disease,it will then perforate and then it will then affect
different organs or blood vessels. If it ispeptic ulcer disease of the stomach which is
usually found in the lesser antrum of the stomach,and if it is to perforate then you are then going to
or the perforation is going to affect the left gastricartery. Whereas if the perforation takes place down
in the duodenum, then the perforation then causesdamage to the gastroduodenal artery. Gastric outlet
obstruction due to peri-pyloric scar formation is animportant complication. At some point in time when
there is enough damage that has taken place,any type of damage at some point, the body wishes to
respond with the repair process. This repair processthat you’re looking for at some point with fibrosis
taking place, may actually then cause gastric outletproblems because of the more or less think of it as
being a stricture formation or a scar formationand therefore decreasing the emptying of the stomach.
Gastric ulcers may be malignant while duodenal ulcersare basically never. Once again, peptic ulcer disease,
keep in mind that if it's the stomach you should bemonitoring or should be thinking, there's possibility
of a primary gastric cancer developing and duodenalalmost never. On the left, the peptic ulcer disease
is in the duodenum. You’ll notice that you have aclean, punched-out lesion. Whereas in gastric
ulcer, you also have a clean, punched-out lesion.
07:02
Endoscopy, Esophagogastroduodenoscopy, would be
your best measure or best method of diagnosis.
07:12
With this ulceration at some point, remember, keep
your ulceration and perforation completely separate.
07:20
Management of peptic ulcer disease. Antacids.
Because of the burning sensation that’s taking place,magnesium and aluminum cause long-term toxicity.
Be careful with antacids, magnesium and aluminum.
07:34
Milk alkali syndrome due to prolonged use of calcium.
A symptom that you want to keep in mind with antacids.
07:40
Once again, milk alkali syndrome due to prolonged
use of calcium. H2 Blockers. Here once again,you block your receptors on histamine for H2 and
decrease acid production if in fact that is one ofyour concerns with peptic ulcer disease. H2 blockers,
however, does inhibit the cytochrome P450 systemin the liver so therefore may then cause decreased
metabolism with certain drugs. So drug-druginteractions become a important side effect. An
interaction that you want to keep in mind for H2 blockers.
08:20
Proton pump inhibitors. Extremely effective in terms
of decreasing the amount of hydrogen that you’repumping into the stomach. Irreversible blockage of
your hydrogen-potassium pump. However, if you areusing this, keep in mind that because you're
decreasing acidity within the stomach, here once again,you might then cause interference of absorption of
other drugs. Drug-drug interactions become incrediblyimportant here. Sucralfate. It stimulates endogenous
prostaglandin productions so that it helps to thenprotect the lining of the stomach. Avoid in
renal insufficiency and that's a big deal.
09:00
So, the drugs that I’ve given here for management,
I’ve given you as to what it does objectivelyand then things that you want to keep in mind as
side effects because these patients will be onthese drugs for quite a bit of time.
09:18
Peptic ulcer disease. We have two types. Duration of
therapy if it’s duodenal ulcer being the most commontype of presentation in the US, 4 to 6 weeks of
duration. If it's gastric ulcer, then it's 6 to 8 weekswith repeated esophagogastroduodenoscopy to document
the healing. The management, remember, H. pylorihighly associated with both of these issues.
Therefore, the importance of eradicating H. pyloricannot be understated. Responsible for developing
lymphomas perhaps and maybe even our intestinaltype of gastric primary adenocarcinoma. Now we
have two types of treatment. So you want toeither think quadruple bismuth. And the quadruple
therapy would inlcude bismuth, metronidazole,tetracycline and proton pump inhibitor. Or you
could have clarithromycin based triple therapywhich would then consist of amoxicillin,
clarithromycin, and your PPI.

About the Lecture

The lecture Peptic Ulcer Disease by Carlo Raj, MD is from the course Stomach and Duodenum Diseases.

Included Quiz Questions

A 75-year-old woman comes to your clinic complaining of constipation, vomiting, and a loss of appetite for the last 4 weeks. She has had a history of peptic ulcer disease for the last ten years, for which she has been on medication intermittently. Which of the following is the most likely cause of her presentation?

Gastric outlet obstruction

Perforation of the ulcer

Ulcer penetration

Bleeding ulcer

GERD

Which of the following pathophysiological mechanisms is not responsible for injury in peptic ulcer disease?

Reflux of acid into the esophageal mucosa

Mucosal damage due to Helicobacter pylori and NSAIDs

Loss of blood supply to mucosa

Increased acid production

Inhibition of prostaglandins

A 35-year-old alcoholic male presents to the emergency department with severe epigastric pain, nausea, and vomiting. His blood pressure is 90/70 mmHg. He is started on intravenous fluids and supportive treatment. After he is stabilized, he states that he was diagnosed with peptic ulcer disease 6 months ago. An endoscopy reveals a bleeding ulcer in the antrum of the stomach. Which of the following is the most likely cause of his symptoms?

Rupture of the left gastric artery

Peri-pyloric scar formation

Malignancy

Rupture of the gastroduodenal artery

Pancreatic bleeding

A 55-year-old male with a history of myocardial infarction and atrial fibrillation presents to your clinic for a refill of cimetidine for his peptic ulcer disease. He is compliant with his medications even though he complains of intermittent epigastric pain, which subsides after meals. A week later he is seen in the emergency room for a nosebleed as well as bleeding in his stools. What is the most likely cause?

Warfarin toxicity due to inhibition of cytochrome P450 by cimetidine

Toxicity of the antacids

Mucosal ischemia due to previous MI

Interaction with proton pump inhibitors

Interaction with sucralfate

A 45-year-old female presents with loss of appetite and fatigue. She has lost a significant amount of weight in the last 4-6 months. Her blood work up shows iron deficiency anemia. She has a prolonged history of peptic ulcer disease. What is the most likely diagnosis and the best treatment option for this patient?

Malignancy due to gastric ulcer disease and antibiotics for H. pylori with follow up EGD

Duodenal ulcer and proton pump inhibitors

Gastro esophageal reflux disease and antacids

Inflammation of the stomach and PPI

Perforated ulcer and endoscopy

Author of lecture Peptic Ulcer Disease

Carlo Raj, MD

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